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Hans Niller
Institute of Medical Microbiology and Hygiene, Molecular Microbiology (Virology), University of Regensburg, Franz-Josef-Strauß-Allee 11, 93053 Regensburg, Germany

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Journal article
Published: 10 June 2021 in Viruses
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SARS-CoV-2 infection fatality ratios (IFR) remain controversially discussed with implications for political measures. The German county of Tirschenreuth suffered a severe SARS-CoV-2 outbreak in spring 2020, with particularly high case fatality ratio (CFR). To estimate seroprevalence, underreported infections, and IFR for the Tirschenreuth population aged ≥14 years in June/July 2020, we conducted a population-based study including home visits for the elderly, and analyzed 4203 participants for SARS-CoV-2 antibodies via three antibody tests. Latent class analysis yielded 8.6% standardized county-wide seroprevalence, a factor of underreported infections of 5.0, and 2.5% overall IFR. Seroprevalence was two-fold higher among medical workers and one third among current smokers with similar proportions of registered infections. While seroprevalence did not show an age-trend, the factor of underreported infections was 12.2 in the young versus 1.7 for ≥85-year-old. Age-specific IFRs were <0.5% below 60 years of age, 1.0% for age 60–69, and 13.2% for age 70+. Senior care homes accounted for 45% of COVID-19-related deaths, reflected by an IFR of 7.5% among individuals aged 70+ and an overall IFR of 1.4% when excluding senior care home residents from our computation. Our data underscore senior care home infections as key determinant of IFR additionally to age, insufficient targeted testing in the young, and the need for further investigations on behavioral or molecular causes of the fewer infections among current smokers.

ACS Style

Ralf Wagner; David Peterhoff; Stephanie Beileke; Felix Günther; Melanie Berr; Sebastian Einhauser; Anja Schütz; Hans Niller; Philipp Steininger; Antje Knöll; Matthias Tenbusch; Clara Maier; Klaus Korn; Klaus Stark; André Gessner; Ralph Burkhardt; Michael Kabesch; Holger Schedl; Helmut Küchenhoff; Annette Pfahlberg; Iris Heid; Olaf Gefeller; Klaus Überla. Estimates and Determinants of SARS-Cov-2 Seroprevalence and Infection Fatality Ratio Using Latent Class Analysis: The Population-Based Tirschenreuth Study in the Hardest-Hit German County in Spring 2020. Viruses 2021, 13, 1118 .

AMA Style

Ralf Wagner, David Peterhoff, Stephanie Beileke, Felix Günther, Melanie Berr, Sebastian Einhauser, Anja Schütz, Hans Niller, Philipp Steininger, Antje Knöll, Matthias Tenbusch, Clara Maier, Klaus Korn, Klaus Stark, André Gessner, Ralph Burkhardt, Michael Kabesch, Holger Schedl, Helmut Küchenhoff, Annette Pfahlberg, Iris Heid, Olaf Gefeller, Klaus Überla. Estimates and Determinants of SARS-Cov-2 Seroprevalence and Infection Fatality Ratio Using Latent Class Analysis: The Population-Based Tirschenreuth Study in the Hardest-Hit German County in Spring 2020. Viruses. 2021; 13 (6):1118.

Chicago/Turabian Style

Ralf Wagner; David Peterhoff; Stephanie Beileke; Felix Günther; Melanie Berr; Sebastian Einhauser; Anja Schütz; Hans Niller; Philipp Steininger; Antje Knöll; Matthias Tenbusch; Clara Maier; Klaus Korn; Klaus Stark; André Gessner; Ralph Burkhardt; Michael Kabesch; Holger Schedl; Helmut Küchenhoff; Annette Pfahlberg; Iris Heid; Olaf Gefeller; Klaus Überla. 2021. "Estimates and Determinants of SARS-Cov-2 Seroprevalence and Infection Fatality Ratio Using Latent Class Analysis: The Population-Based Tirschenreuth Study in the Hardest-Hit German County in Spring 2020." Viruses 13, no. 6: 1118.

Journal article
Published: 07 April 2021 in Cancers
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In recent years, onco-metabolites like D-2-hydroxyglutarate, which is produced in isocitrate dehydrogenase-mutated tumors, have gained increasing interest. Here, we report a metabolite in human specimens that is closely related to 2-hydroxyglutarate: the intramolecular ester of 2-hydroxyglutarate, 2-hydroxyglutarate-γ-lactone. Using 13C5-L-glutamine tracer analysis, we showed that 2-hydroxyglutarate is the endogenous precursor of 2-hydroxyglutarate-lactone and that there is a high exchange between these two metabolites. Lactone formation does not depend on mutated isocitrate dehydrogenase, but its formation is most probably linked to transport processes across the cell membrane and favored at low environmental pH. Furthermore, human macrophages showed not only striking differences in uptake of 2-hydroxyglutarate and its lactone but also in the enantiospecific hydrolysis of the latter. Consequently, 2-hydroxyglutarate-lactone may play a critical role in the modulation of the tumor microenvironment.

ACS Style

Raffaela Berger; Christian Wachsmuth; Magdalena Waldhier; Kathrin Renner-Sattler; Simone Thomas; Anuhar Chaturvedi; Hans-Helmut Niller; Elisabeth Bumes; Peter Hau; Martin Proescholdt; Wolfram Gronwald; Michael Heuser; Marina Kreutz; Peter Oefner; Katja Dettmer. Lactonization of the Oncometabolite D-2-Hydroxyglutarate Produces a Novel Endogenous Metabolite. Cancers 2021, 13, 1756 .

AMA Style

Raffaela Berger, Christian Wachsmuth, Magdalena Waldhier, Kathrin Renner-Sattler, Simone Thomas, Anuhar Chaturvedi, Hans-Helmut Niller, Elisabeth Bumes, Peter Hau, Martin Proescholdt, Wolfram Gronwald, Michael Heuser, Marina Kreutz, Peter Oefner, Katja Dettmer. Lactonization of the Oncometabolite D-2-Hydroxyglutarate Produces a Novel Endogenous Metabolite. Cancers. 2021; 13 (8):1756.

Chicago/Turabian Style

Raffaela Berger; Christian Wachsmuth; Magdalena Waldhier; Kathrin Renner-Sattler; Simone Thomas; Anuhar Chaturvedi; Hans-Helmut Niller; Elisabeth Bumes; Peter Hau; Martin Proescholdt; Wolfram Gronwald; Michael Heuser; Marina Kreutz; Peter Oefner; Katja Dettmer. 2021. "Lactonization of the Oncometabolite D-2-Hydroxyglutarate Produces a Novel Endogenous Metabolite." Cancers 13, no. 8: 1756.

Review article
Published: 29 May 2019 in Infection, Genetics and Evolution
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Members of the virus families Retroviridae and Hepadnaviridae use reverse transcriptase (RT) to synthesize a DNA copy of their genomic and pregenomic RNA, respectively, during the viral life cycle. A group of viruses belonging to Retroviridae (“acute transforming” retroviruses) as well as human hepatitis B virus (HBV), the prototype member of Hepadnaviridae (hepadnaviruses) are able to cause malignant neoplasms in infected hosts, due to the expression of pleiotropic “transforming proteins” encoded by the genomes of these reverse-transcribing tumor viruses. In this review we wish to compare the common and unique features of replication strategies characteristic of acute transforming retroviruses and HBV and summarize data related to the origin and evolution of their viral oncogenes either via transduction of cellular genes, or by accumulation of mutations in viral sequences that create a new open reading frame (overprinting). The exons of cellular genes (proto-onc genes or c-onc genes) incorporated into the genome of acute transforming retroviruses are regularly affected by deletions resulting in the expression of truncated viral oncoproteins which are frequently dysregulated compared to their cellular counterparts. These retroviral transforming proteins alter the behavior of their target cells (malignant transformation). HBx, a pleiotropic protein of HBV, regulates virus replication and contributes to hepatocarcinogenesis. In contrast to the v-onc genes of acute transforming retroviruses, the viral gene encoding the full-length, wild-type HBx (wtHBx) protein does not have a cellular counterpart. Mutations and deletions frequently affect, however, the HBV genome as well, resulting in the expression of truncated HBx proteins (trHBx) in liver cells. Truncated, especially C-terminal truncated variants of HBx (Ct-HBX proteins), may facilitate initiation and progression of liver carcinoma.

ACS Style

Janos Minarovits; Hans Helmut Niller. Truncated oncoproteins of retroviruses and hepatitis B virus: A lesson in contrasts. Infection, Genetics and Evolution 2019, 73, 342 -357.

AMA Style

Janos Minarovits, Hans Helmut Niller. Truncated oncoproteins of retroviruses and hepatitis B virus: A lesson in contrasts. Infection, Genetics and Evolution. 2019; 73 ():342-357.

Chicago/Turabian Style

Janos Minarovits; Hans Helmut Niller. 2019. "Truncated oncoproteins of retroviruses and hepatitis B virus: A lesson in contrasts." Infection, Genetics and Evolution 73, no. : 342-357.

Book chapter
Published: 28 March 2018 in Cellular Ecophysiology of Microbe: Hydrocarbon and Lipid Interactions
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In this chapter we focus on the regulation and function of DNA methylation in mammals and especially in humans. We describe the main features of the enzymatic machinery generating 5-methylcytosine (5mC) that functions as an epigenetic mark in mammalian cells, and outline the active and passive mechanisms that can remove this reversible modification of DNA. We briefly introduce the characteristics of “maintenance” and “de novo” DNA-(cytosine-C5)-methyltransferases (DNMTs) and overview how their expression is regulated at the transcriptional, posttranscriptional, and posttranslational level. The interacting partners and chromatin marks involved in the targeting of DNMTs to the replication foci during S phase or to various chromatin domains during other phases of the cell cycle are also discussed. The enzymatic functions of DNMTs and their interactions with cellular macromolecules are involved in a series of cellular processes, some of them vital for mammals. Thus, DNA methylation has a role in the regulation of chromatin structure and promoter activity. It may silence the promoters of imprinted genes showing monoallelic expression as well as the promoters of transposons, and contributes to gene silencing on the inactive X chromosome, too. There are genome-wide demethylation and remethylation events during embryogenesis suggesting a regulatory role for DNA methylation in developmental processes, and both cytosine methylation and the active removal of 5mC from DNA is involved in the control of cell differentiation. DNA methylation plays a role in the preservation of genomic stability and gene body methylation affects the inclusion of certain exons into mature mRNA molecules by affecting – indirectly – the splicing of primary transcripts. Epigenetic regulatory mechanisms, including DNA methylation, are at the forefront of brain research these days. For this reason we outlined some of the most interesting results of this exciting new field in a separate subsection.

ACS Style

Hans Helmut Niller; Anett Demcsák; Janos Minarovits. DNA Methylation in Eukaryotes: Regulation and Function. Cellular Ecophysiology of Microbe: Hydrocarbon and Lipid Interactions 2018, 509 -570.

AMA Style

Hans Helmut Niller, Anett Demcsák, Janos Minarovits. DNA Methylation in Eukaryotes: Regulation and Function. Cellular Ecophysiology of Microbe: Hydrocarbon and Lipid Interactions. 2018; ():509-570.

Chicago/Turabian Style

Hans Helmut Niller; Anett Demcsák; Janos Minarovits. 2018. "DNA Methylation in Eukaryotes: Regulation and Function." Cellular Ecophysiology of Microbe: Hydrocarbon and Lipid Interactions , no. : 509-570.

Book chapter
Published: 01 January 2018 in Epigenetics in Human Disease
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ACS Style

Neha Aggarwal; Yasuto Araki; Erfan Aref-Eshghi; Takahiro Arima; Yunfeng Bai; Bahar Barani; Megan Beetch; Georgina E.T. Blake; Graham C. Burdge; Deanna Alexis Carere; Pearl Chang; Pao-Yang Chen; Mariano Colón-Caraballo; Fabio Coppedè; Buddhadeb Dawn; Pierre-Antoine Dugué; Sarah El-Heis; Eliana Portilla Fernandez; Idhaliz Flores-Caldera; Oscar H. Franco; Andrea Fuso; Mohsen Ghanbari; Asish K. Ghosh; Peter D. Gluckman; Keith M. Godfrey; Moloya Gohain; Steven G. Gray; Mark A. Hanson; Hiromitsu Hattori; Christian M. Hedrich; Hitoshi Hiura; John L. Hopper; Amir Hosseini; Cathrine Hoyo; Fei-Man Hsu; Wilfried Karmaus; Norio Kobayashi; Jannet Kocerha; Alexander K. Koliada; Leila Larijani; Sophie A. Lelievre; Shuai Li; Karen A. Lillycrop; Jui-Hsien Lu; Katarzyna Lubecka; Oleh V. Lushchak; Masato Maekawa; Amanda H. Mahnke; Giuseppina Mastrototaro; Roger L. Milne; Toshihide Mimura; Janos Minarovits; Saverio Minucci; Rajesh C. Miranda; Vasavi Mohan; Taulant Muka; Nandini Mukherjee; Apiwat Mutirangura; Jana Nano; Khue Vu Nguyen; Hans Helmut Niller; Hiroaki Okae; Sarah S. Park; Kamthorn Pruksananonda; Sheeja Rajasingh; Johnson Rajasingh; Joanna Rakoczy; Derrick E. Rancourt; David I. Rodenhiser; Bekim Sadikovic; Sabita N. Saldanha; Nihal A. Salem; Saheli Samanta; Laila C. Schenkel; Alessandro Sessa; David A. Skaar; Patricia Sorrow; Barbara Stefanska; Souta Takahashi; Sravya Thumoju; Trygve O. Tollefsbol; Jenna Troup; Alexander M. Tseng; Alexander M. Vaiserman; Douglas E. Vaughan; Sumei Wang; Ruilan Wang; ArtisA Wasinarom; Yoshihisa Watanabe; Erica D. Watson; Wanyin Wu; Zhigang Zhou; Ali H. Ziyab. List of Contributors. Epigenetics in Human Disease 2018, 1 .

AMA Style

Neha Aggarwal, Yasuto Araki, Erfan Aref-Eshghi, Takahiro Arima, Yunfeng Bai, Bahar Barani, Megan Beetch, Georgina E.T. Blake, Graham C. Burdge, Deanna Alexis Carere, Pearl Chang, Pao-Yang Chen, Mariano Colón-Caraballo, Fabio Coppedè, Buddhadeb Dawn, Pierre-Antoine Dugué, Sarah El-Heis, Eliana Portilla Fernandez, Idhaliz Flores-Caldera, Oscar H. Franco, Andrea Fuso, Mohsen Ghanbari, Asish K. Ghosh, Peter D. Gluckman, Keith M. Godfrey, Moloya Gohain, Steven G. Gray, Mark A. Hanson, Hiromitsu Hattori, Christian M. Hedrich, Hitoshi Hiura, John L. Hopper, Amir Hosseini, Cathrine Hoyo, Fei-Man Hsu, Wilfried Karmaus, Norio Kobayashi, Jannet Kocerha, Alexander K. Koliada, Leila Larijani, Sophie A. Lelievre, Shuai Li, Karen A. Lillycrop, Jui-Hsien Lu, Katarzyna Lubecka, Oleh V. Lushchak, Masato Maekawa, Amanda H. Mahnke, Giuseppina Mastrototaro, Roger L. Milne, Toshihide Mimura, Janos Minarovits, Saverio Minucci, Rajesh C. Miranda, Vasavi Mohan, Taulant Muka, Nandini Mukherjee, Apiwat Mutirangura, Jana Nano, Khue Vu Nguyen, Hans Helmut Niller, Hiroaki Okae, Sarah S. Park, Kamthorn Pruksananonda, Sheeja Rajasingh, Johnson Rajasingh, Joanna Rakoczy, Derrick E. Rancourt, David I. Rodenhiser, Bekim Sadikovic, Sabita N. Saldanha, Nihal A. Salem, Saheli Samanta, Laila C. Schenkel, Alessandro Sessa, David A. Skaar, Patricia Sorrow, Barbara Stefanska, Souta Takahashi, Sravya Thumoju, Trygve O. Tollefsbol, Jenna Troup, Alexander M. Tseng, Alexander M. Vaiserman, Douglas E. Vaughan, Sumei Wang, Ruilan Wang, ArtisA Wasinarom, Yoshihisa Watanabe, Erica D. Watson, Wanyin Wu, Zhigang Zhou, Ali H. Ziyab. List of Contributors. Epigenetics in Human Disease. 2018; ():1.

Chicago/Turabian Style

Neha Aggarwal; Yasuto Araki; Erfan Aref-Eshghi; Takahiro Arima; Yunfeng Bai; Bahar Barani; Megan Beetch; Georgina E.T. Blake; Graham C. Burdge; Deanna Alexis Carere; Pearl Chang; Pao-Yang Chen; Mariano Colón-Caraballo; Fabio Coppedè; Buddhadeb Dawn; Pierre-Antoine Dugué; Sarah El-Heis; Eliana Portilla Fernandez; Idhaliz Flores-Caldera; Oscar H. Franco; Andrea Fuso; Mohsen Ghanbari; Asish K. Ghosh; Peter D. Gluckman; Keith M. Godfrey; Moloya Gohain; Steven G. Gray; Mark A. Hanson; Hiromitsu Hattori; Christian M. Hedrich; Hitoshi Hiura; John L. Hopper; Amir Hosseini; Cathrine Hoyo; Fei-Man Hsu; Wilfried Karmaus; Norio Kobayashi; Jannet Kocerha; Alexander K. Koliada; Leila Larijani; Sophie A. Lelievre; Shuai Li; Karen A. Lillycrop; Jui-Hsien Lu; Katarzyna Lubecka; Oleh V. Lushchak; Masato Maekawa; Amanda H. Mahnke; Giuseppina Mastrototaro; Roger L. Milne; Toshihide Mimura; Janos Minarovits; Saverio Minucci; Rajesh C. Miranda; Vasavi Mohan; Taulant Muka; Nandini Mukherjee; Apiwat Mutirangura; Jana Nano; Khue Vu Nguyen; Hans Helmut Niller; Hiroaki Okae; Sarah S. Park; Kamthorn Pruksananonda; Sheeja Rajasingh; Johnson Rajasingh; Joanna Rakoczy; Derrick E. Rancourt; David I. Rodenhiser; Bekim Sadikovic; Sabita N. Saldanha; Nihal A. Salem; Saheli Samanta; Laila C. Schenkel; Alessandro Sessa; David A. Skaar; Patricia Sorrow; Barbara Stefanska; Souta Takahashi; Sravya Thumoju; Trygve O. Tollefsbol; Jenna Troup; Alexander M. Tseng; Alexander M. Vaiserman; Douglas E. Vaughan; Sumei Wang; Ruilan Wang; ArtisA Wasinarom; Yoshihisa Watanabe; Erica D. Watson; Wanyin Wu; Zhigang Zhou; Ali H. Ziyab. 2018. "List of Contributors." Epigenetics in Human Disease , no. : 1.

Book chapter
Published: 01 January 2018 in Epigenetics in Human Disease
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Certain bacterial and viral infections regularly cause epigenetic alterations in host cells. Porphyromonas gingivalis secretes butyric acid, an inhibitor of histone deacetylases (HDACs), and may thereby elicit increased acetylation of histones H3 and H4 in the cells of the oral cavity. Listeriolysin O, a toxin secreted by Listeria monocytogenes, induces dephosphorylation of histone H3 at promoters of defense genes, thereby interfering with innate immunity. Other bacterial toxins and the OspF effector protein of Shigella flexneri also modulate histone H3 phosphorylation. The L. monocytogenes surface protein InlB silences immune-regulatory genes by eliciting translocation of SIRT2, an HDAC, into the host cell nuclei. AnkA, the effector protein of Anaplasma phagocytophilum achieves a similar effect by upregulating HDACs in granulocytes. DNA-(cytosine C5)-methyltransferases of Mycoplasma hyorhinis and Mycobacterium tuberculosis directly target cytosines of the infected host cell DNA. Hypermethylation of key cellular promoters at CpG dinucleotides, first observed in human immunodeficiency virus–infected cells, plays an important role in neoplastic development associated with Helicobacter pylori, Epstein–Barr virus, Kaposi's sarcoma-associated herpesvirus, human T-cell lymphotropic virus, hepatitis B virus, hepatitis C virus, and the macroparasite trematodes Opistorchis viverrini and Schistosoma haematobium, whereas the human papillomavirus oncoprotein E7 induces both histone methyltransferase and histone demethylase enzymes. Elucidation of patho-epigenetic consequences of microbe–host interactions may help to design new diagnostic tools and therapeutic strategies.

ACS Style

Hans Helmut Niller; Janos Minarovits. Epigenetics and Human Infectious Diseases. Epigenetics in Human Disease 2018, 643 -687.

AMA Style

Hans Helmut Niller, Janos Minarovits. Epigenetics and Human Infectious Diseases. Epigenetics in Human Disease. 2018; ():643-687.

Chicago/Turabian Style

Hans Helmut Niller; Janos Minarovits. 2018. "Epigenetics and Human Infectious Diseases." Epigenetics in Human Disease , no. : 643-687.

Review
Published: 01 June 2017 in Current Opinion in Infectious Diseases
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We wished to overview recent data on a subset of epigenetic changes elicited by intracellular bacteria in human cells. Reprogramming the gene expression pattern of various host cells may facilitate bacterial growth, survival, and spread. DNA-(cytosine C5)-methyltransferases of Mycoplasma hyorhinis targeting cytosine-phosphate-guanine (CpG) dinucleotides and a Mycobacterium tuberculosis methyltransferase targeting non-CpG sites methylated the host cell DNA and altered the pattern of gene expression. Gene silencing by CpG methylation and histone deacetylation, mediated by cellular enzymes, also occurred in M. tuberculosis-infected macrophages. M. tuberculosis elicited cell type-specific epigenetic changes: it caused increased DNA methylation in macrophages, but induced demethylation, deposition of euchromatic histone marks and activation of immune-related genes in dendritic cells. A secreted transposase of Acinetobacter baumannii silenced a cellular gene, whereas Mycobacterium leprae altered the epigenotype, phenotype, and fate of infected Schwann cells. The ‘keystone pathogen’ oral bacterium Porphyromonas gingivalis induced local DNA methylation and increased the level of histone acetylation in host cells. These epigenetic changes at the biofilm–gingiva interface may contribute to the development of periodontitis. Epigenetic regulators produced by intracellular bacteria alter the epigenotype and gene expression pattern of host cells and play an important role in pathogenesis.

ACS Style

Hans Helmut Niller; Roland Masa; Annamária Venkei; Sándor Mészáros; Janos Minarovits. Pathogenic mechanisms of intracellular bacteria. Current Opinion in Infectious Diseases 2017, 30, 309 -315.

AMA Style

Hans Helmut Niller, Roland Masa, Annamária Venkei, Sándor Mészáros, Janos Minarovits. Pathogenic mechanisms of intracellular bacteria. Current Opinion in Infectious Diseases. 2017; 30 (3):309-315.

Chicago/Turabian Style

Hans Helmut Niller; Roland Masa; Annamária Venkei; Sándor Mészáros; Janos Minarovits. 2017. "Pathogenic mechanisms of intracellular bacteria." Current Opinion in Infectious Diseases 30, no. 3: 309-315.

Journal article
Published: 01 January 2017 in Journal of Microbial & Biochemical Technology
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Lamin A, B and C, the nuclear intermediate-filament proteins, play a role in epigenetic regulation. Lamin B could be detected in all nucleated cells studied, whereas the lamin A and lamin C isoforms (lamin A/C) encoded by the LMNA gene are co-expressed in most somatic cell types except mature B lymphocytes. Since Epstein-Barr virus (EBV), a human gammaherpesvirus, is associated with tumorigenic processes and is known to alter the epigenotype of its host cells, we studied the expression of the LMNA gene and its epigenetic marks in EBV-carrying human lymphoid cell lines. We observed a high lamin A/C mRNA expression in EBV-immortalized B lymphoblastoid cell lines (LCLs) and in a subset of Burkitt lymphoma (BL) lines characterized by an activated B cell phenotype and a unique latent EBV gene expression pattern (latency III). In these cells the first exon of LMNA was hypomethylated and associated with activating histone marks. In contrast, we observed a low level of lamin A/C mRNA expression in EBV negative BL lines and BL lines with a restricted expression of latent EBV products (latency I). Low LMNA promoter activity was associated with hypermethylation of the LMNA first exon. These data suggest a role for EBV latency products in switching on or upregulating the LMNA promoter (LMNAp) in EBV-infected activated B cells in vitro. Lamin A/C may contribute to the establishment of the activated B cell phenotype. Our data also imply a role of LMNA first exon methylation in the silencing of LMNAp.

ACS Style

Ferenc Banati; Anita Koroknai; Anita Hidasi; Barbara Bankuti; Frederic Lemnitzer; Zsolt Ruzsics; Susan Szathmary; Hans Wolf; Daniel Salamon; Janos Minarovits; Hans Helmut Niller; Kalman Szenthe; Tamas Tereh; Krisztina Buzas. Up-Regulation of Lamin A/C Expression in Epstein-Barr Virus Immortalized B Cells and Burkitt Lymphoma Cell Lines of Activated B Cell Phenotype. Journal of Microbial & Biochemical Technology 2017, 9, 1 .

AMA Style

Ferenc Banati, Anita Koroknai, Anita Hidasi, Barbara Bankuti, Frederic Lemnitzer, Zsolt Ruzsics, Susan Szathmary, Hans Wolf, Daniel Salamon, Janos Minarovits, Hans Helmut Niller, Kalman Szenthe, Tamas Tereh, Krisztina Buzas. Up-Regulation of Lamin A/C Expression in Epstein-Barr Virus Immortalized B Cells and Burkitt Lymphoma Cell Lines of Activated B Cell Phenotype. Journal of Microbial & Biochemical Technology. 2017; 9 (3):1.

Chicago/Turabian Style

Ferenc Banati; Anita Koroknai; Anita Hidasi; Barbara Bankuti; Frederic Lemnitzer; Zsolt Ruzsics; Susan Szathmary; Hans Wolf; Daniel Salamon; Janos Minarovits; Hans Helmut Niller; Kalman Szenthe; Tamas Tereh; Krisztina Buzas. 2017. "Up-Regulation of Lamin A/C Expression in Epstein-Barr Virus Immortalized B Cells and Burkitt Lymphoma Cell Lines of Activated B Cell Phenotype." Journal of Microbial & Biochemical Technology 9, no. 3: 1.

Preprint
Published: 24 November 2016
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Lamin A, B and C, the nuclear intermediate-filament proteins, play a role in epigenetic regulation. While Lamin B is expressed in all nucleated cells studied, Lamin A/C are transcribed in most somatic cell types except mature B lymphocytes. Since Epstein-Barr virus (EBV), a human gammaherpesvirus, is associated with tumorigenic processes and is known to alter the epigenotype of its host cells, we studied the expression of the LMNA gene and its epigenetic marks in EBV-carrying human lymphoid cell lines. We observed a high lamin A/C mRNA and protein expression in EBV-immortalized lymphoblastoid cell lines (LCLs) and in group III Burkitt lymphoma (BL) lines where hypomethylated first exons were observed with activating histone marks. In most cell lines with low promoter activity a highly methylated first exon could be detected. Our data showed that methylation of the first exon of LMNA was associated with the downregulation of LMNA expression whereas euchromatic histone marks were enriched at active LMNA promoters in EBV-immortalized LCLs. These data suggest a role for viral latency products to activate LMNAp in EBV-infected latency type III B cells in vitro. Expression of lamin A/C may contribute to the establishment of activated B cell phenotype that needs further explorations.

ACS Style

Ferenc Bánáti; Anita Koroknai; Kálmán Szenthe; Tamás Tereh; Nóra Kovács; Anita Hidasi; Barbara Bánkuti; Krisztina Buzás; Frederic Lemnitzer; Zsolt Ruzsics; Susan Szathmary; Hans Wolf; Dániel Salamon; János Minárovits; Hans-Helmut Niller. Up-regulation of Lamin A/C Expression in Epstein-Barr Virus Immortalized B Cells and Burkitt Lymphoma Cell Lines of Activated B Cell Phenotype. 2016, 1 .

AMA Style

Ferenc Bánáti, Anita Koroknai, Kálmán Szenthe, Tamás Tereh, Nóra Kovács, Anita Hidasi, Barbara Bánkuti, Krisztina Buzás, Frederic Lemnitzer, Zsolt Ruzsics, Susan Szathmary, Hans Wolf, Dániel Salamon, János Minárovits, Hans-Helmut Niller. Up-regulation of Lamin A/C Expression in Epstein-Barr Virus Immortalized B Cells and Burkitt Lymphoma Cell Lines of Activated B Cell Phenotype. . 2016; ():1.

Chicago/Turabian Style

Ferenc Bánáti; Anita Koroknai; Kálmán Szenthe; Tamás Tereh; Nóra Kovács; Anita Hidasi; Barbara Bánkuti; Krisztina Buzás; Frederic Lemnitzer; Zsolt Ruzsics; Susan Szathmary; Hans Wolf; Dániel Salamon; János Minárovits; Hans-Helmut Niller. 2016. "Up-regulation of Lamin A/C Expression in Epstein-Barr Virus Immortalized B Cells and Burkitt Lymphoma Cell Lines of Activated B Cell Phenotype." , no. : 1.

Case reports
Published: 22 November 2016 in Methods in Molecular Biology
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The vast majority of the human adult population is infected with Epstein-Barr virus (EBV), and the majority of the EBV-infected individuals tolerates the infection well, without any further symptoms after primary infection. In cases of individuals which undergo primary infection in the form of an infectious mononucleosis, or which have undergone primary infection in their past, it is sometimes important to appraise symptomatic disease or differentiate infectious mononucleosis from other conditions. In these cases, serological methods, i.e., immunofluorescence, ELISA, or Western blot, are the methods of choice to come to an unequivocal diagnostic conclusion, while the detection and quantification of viral DNA through PCR plays a minor role. On the other hand, in a minority of the human population, EBV infection is associated or causally linked with autoimmune or malignant disease. Especially in the bone marrow or solid organ transplanted, or in otherwise severely immune-suppressed patients, prolonged EBV primary infection or EBV reactivation from latency may be a serious and life-threatening complication which needs to be diagnosed the faster the better, in order to take therapeutic steps in time. Determining the serostatus correctly is also important in these cases. However, the direct and quantitative detection of viral DNA are of importance for the diagnosis of serious EBV disease and its monitoring. In the following, we give an overview of diagnostic methods to accurately determine EBV serostatus and viral load. We evaluate the advantages and disadvantages of each method and report on the diagnostic significance of each and how to resolve diagnostic problems in case of uncertainties. For practical procedures, we refer to the detailed instruction manuals of the respective test kit manufacturers which have to be closely followed for reliable results.

ACS Style

Hans-Helmut Niller; Georg Bauer. Epstein-Barr Virus: Clinical Diagnostics. Methods in Molecular Biology 2016, 1532, 33 -55.

AMA Style

Hans-Helmut Niller, Georg Bauer. Epstein-Barr Virus: Clinical Diagnostics. Methods in Molecular Biology. 2016; 1532 ():33-55.

Chicago/Turabian Style

Hans-Helmut Niller; Georg Bauer. 2016. "Epstein-Barr Virus: Clinical Diagnostics." Methods in Molecular Biology 1532, no. : 33-55.

Journal article
Published: 01 January 2016 in Single Molecule and Single Cell Sequencing
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ACS Style

Janos Minarovits; Hans Helmut Niller. Epigenetic regulatory mechanisms ensure the heritable alterations of cellular states. Introduction. Single Molecule and Single Cell Sequencing 2016, 879, 1 .

AMA Style

Janos Minarovits, Hans Helmut Niller. Epigenetic regulatory mechanisms ensure the heritable alterations of cellular states. Introduction. Single Molecule and Single Cell Sequencing. 2016; 879 ():1.

Chicago/Turabian Style

Janos Minarovits; Hans Helmut Niller. 2016. "Epigenetic regulatory mechanisms ensure the heritable alterations of cellular states. Introduction." Single Molecule and Single Cell Sequencing 879, no. : 1.

Chapter
Published: 12 December 2015 in Advances in Experimental Medicine and Biology
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Some of the key epigenetic regulatory mechanisms appeared early during evolution, and the acquisition of novel epigenetic regulators apparently facilitated certain evolutionary transitions. In this short review we focus mainly on the major epigenetic mechanisms that control chromatin structure and accessibility in mammalian cells. The enzymes methylating CpG dinucleotides and those involved in the active demethylation of 5-metylcytosine (5mC) are outlined together with the members of the methyl binding protein (MBP) family that bind to and “interpret” the 5mC mark. The enzymes involved in reversible, covalent modifications of core histone proteins that affect chromatin structure are also described briefly. Proteins that build up Polycomb group (PcG) and Trithorax group (TrxG) protein complexes may also modify histones. By establishing heritable chromatin states, PcG and TrxG complexes contribute – similarly to cytosine methylation – to the transmission of cell type-specific gene expression patterns from cell generation to cell generation. Novel players involved in epigenetic regulation, including variant histones, pioneer transcription factors, long noncoding RNA molecules and the regulators of long-distance chromatin interactions are introduced as well, followed by the characterization of various chromatin types.

ACS Style

Janos Minarovits; Ferenc Banati; Kalman Szenthe; Hans Helmut Niller. Epigenetic Regulation. Advances in Experimental Medicine and Biology 2015, 879, 1 -25.

AMA Style

Janos Minarovits, Ferenc Banati, Kalman Szenthe, Hans Helmut Niller. Epigenetic Regulation. Advances in Experimental Medicine and Biology. 2015; 879 ():1-25.

Chicago/Turabian Style

Janos Minarovits; Ferenc Banati; Kalman Szenthe; Hans Helmut Niller. 2015. "Epigenetic Regulation." Advances in Experimental Medicine and Biology 879, no. : 1-25.

Chapter
Published: 12 December 2015 in Advances in Experimental Medicine and Biology
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The oncoproteins of human tumor viruses regularly interact with the cellular epigenetic machinery. Such interactions alter the epigenome of the host cell and reprogram its gene expression pattern. Altered levels or redistribution of (cytosine-5)-DNA methyltransferases and changes in the cellular methylome were observed in Kaposi sarcoma-associated herpesvirus (KSHV), hepatitis B virus (HBV), hepatitis D virus (HDV), hepatitis C virus (HCV), and human papillomavirus (HPV) associated neoplasms and cell lines. Methylation-mediated silencing of cellular promoters was also noted in Merkel cell polyomavirus (MCPyV) positive Merkel cell carcinomas, and, as discussed elsewhere, in EBV-associated malignancies and adenovirus-induced rodent tumors as well. Promoter activation also occurred, either associated with DNA hypomethylation or with the induction of euchromatic histone modifications by viral oncoproteins. It is worthy to notice that HCV infection induced large, hypomethylated blocks of cellular chromatin, although the exact molecular mechanism remains to be elucidated. In hepatoma cells expressing HBx, the oncoprotein encoded by the HBV genome, demethylation of the repetitive satellite 2 sequences was observed, due to downregulation of the de novo DNA methyltransferase DNMT3B. Tax and HBZ, the oncoproteins of human T-cell lymphotropic virus type I (HTLV-I), can both activate and silence distinct cellular promoters by interacting with cellular enzymes involved in histone modification.

ACS Style

Janos Minarovits; Anett Demcsák; Ferenc Banati; Hans Helmut Niller. Epigenetic Dysregulation in Virus-Associated Neoplasms. Advances in Experimental Medicine and Biology 2015, 879, 71 -90.

AMA Style

Janos Minarovits, Anett Demcsák, Ferenc Banati, Hans Helmut Niller. Epigenetic Dysregulation in Virus-Associated Neoplasms. Advances in Experimental Medicine and Biology. 2015; 879 ():71-90.

Chicago/Turabian Style

Janos Minarovits; Anett Demcsák; Ferenc Banati; Hans Helmut Niller. 2015. "Epigenetic Dysregulation in Virus-Associated Neoplasms." Advances in Experimental Medicine and Biology 879, no. : 71-90.

Review
Published: 23 November 2015 in Reviews in Medical Virology
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Hepatitis B virus (HBV) is one of the causative agents of hepatocellular carcinoma. The molecular mechanisms of tumorigenesis are complex. One of the host factors involved is apparently the long-lasting inflammatory reaction which accompanies chronic HBV infection. Although HBV lacks a typical viral oncogene, the HBx gene encoding a pleiotropic regulatory protein emerged as a major player in liver carcinogenesis. Here we review the tumorigenic functions of HBx with an emphasis on wild type and truncated HBx variants, and their role in the transcriptional dysregulation and epigenetic reprogramming of the host cell genome. We suggest that HBx acquired by the HBV genome during evolution acts like a cellular proto-onc gene that is activated by deletion during hepatocarcinogenesis. The resulting viral oncogene (v-onc gene) codes for a truncated HBx protein that facilitates tumor progression. Copyright © 2015 John Wiley & Sons, Ltd.

ACS Style

Hans Helmut Niller; Eva Ay; Ferenc Banati; Anett Demcsák; Maria Takacs; Janos Minarovits. Wild type HBx and truncated HBx: Pleiotropic regulators driving sequential genetic and epigenetic steps of hepatocarcinogenesis and progression of HBV-associated neoplasms. Reviews in Medical Virology 2015, 26, 57 -73.

AMA Style

Hans Helmut Niller, Eva Ay, Ferenc Banati, Anett Demcsák, Maria Takacs, Janos Minarovits. Wild type HBx and truncated HBx: Pleiotropic regulators driving sequential genetic and epigenetic steps of hepatocarcinogenesis and progression of HBV-associated neoplasms. Reviews in Medical Virology. 2015; 26 (1):57-73.

Chicago/Turabian Style

Hans Helmut Niller; Eva Ay; Ferenc Banati; Anett Demcsák; Maria Takacs; Janos Minarovits. 2015. "Wild type HBx and truncated HBx: Pleiotropic regulators driving sequential genetic and epigenetic steps of hepatocarcinogenesis and progression of HBV-associated neoplasms." Reviews in Medical Virology 26, no. 1: 57-73.

Mini review article
Published: 21 October 2014 in Frontiers in Genetics
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Epstein-Barr virus (EBV) is associated with diverse lymphoid and epithelial malignancies. Their molecular pathogenesis is accompanied by epigenetic alterations which are distinct for each of them. While lymphoblastoid cell lines (LCLs) derived from B cells transformed by EBV in vitro are characterized by a massive demethylation and euchromatinization of the viral and cellular genomes, the primarily malignant lymphoid tumour Burkitt’s lymphoma (BL) and the epithelial tumours nasopharyngeal carcinoma (NPC) and EBV-associated gastric carcinoma (EBVaGC) are characterized by hypermethylation of a multitude of cellular tumour suppressor gene loci and of the viral genomes. In some cases, the viral latency and oncoproteins including the latent membrane proteins LMP1 and LMP2A and several nuclear antigens (EBNAs) affect the level of cellular DNA methyltansferases or interact with the histone modifying machinery. Specific molecular mechanisms of the epigenetic dialogue between virus and host cell remain to be elucidated.

ACS Style

Hans H. Niller; Kalman Szenthe; Janos Minarovits. Epstein–Barr virus–host cell interactions: an epigenetic dialog? Frontiers in Genetics 2014, 5, 367 -367.

AMA Style

Hans H. Niller, Kalman Szenthe, Janos Minarovits. Epstein–Barr virus–host cell interactions: an epigenetic dialog? Frontiers in Genetics. 2014; 5 ():367-367.

Chicago/Turabian Style

Hans H. Niller; Kalman Szenthe; Janos Minarovits. 2014. "Epstein–Barr virus–host cell interactions: an epigenetic dialog?" Frontiers in Genetics 5, no. : 367-367.

Journal article
Published: 01 January 2014 in Journal of NasoPharyngeal Carcinoma
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Epstein-Barr virus (EBV) is associated with diverse hematological and epithelial malignancies, such as Burkitt lymphoma, Hodgkin lymphoma, nasopharyngeal carcinoma, gastric carcinoma, and others. Upon infection of B‑lymphoid and epithelial cells, the virus adopts distinct gene expression patterns which depend on the cellular epigenetic machinery. Moreover, virus infection regularly induces modifications of the viral and host cell transcriptomes and epigenomes through the interaction of viral proteins with cellular epigenetic regulators. Viral latent and immediate early proteins may principally contribute to the reprogramming of the cellular epigenome. While EBV-immortalized B lymphoblastoid cell lines are characterized by a massive hypomethylation of the cellular genome and genome-wide reorganization and loss of heterochromatic histone marks, EBV associated malignancies are characterized by local hypermethylation of CpG islands (CGI) at specific gene sets characteristic for each tumor type. Groups of hypermethylated promoters may represent unique EBV associated epigenetic signatures in EBV-associated gastric carcinomas (EBVaGC) and nasopharyngeal carcinomas (NPC). Here, we review the similarities and differences between EBVaGC and NPC with an emphasis on the epigenetic perspective. Both tumors exhibit a CpG island methylator phenotype (CIMP) and a very high load of hypermethylated tumor suppressor genes, EBVaGC more so than the EBV-negative GC subtypes. However, according to present knowledge, there is only a very small set of hypermethylated gene loci which EBVaGC and NPC have in common. Construction of whole genome comparative methylomes and genome-wide analysis of further epigenetic marks may illuminate the patho-epigenetics of these EBV-associated carcinomas.

ACS Style

Niller Hans-Helmut; Banati Ferenc; Minarovits Janos; Hans-Helmut Niller; Ferenc Banati; Janos Minarovits. Epigenetic alterations in nasopharyngeal carcinoma and Epstein-Barr virus (EBV) associated gastric carcinoma: a lesson in contrasts. Journal of NasoPharyngeal Carcinoma 2014, 1 .

AMA Style

Niller Hans-Helmut, Banati Ferenc, Minarovits Janos, Hans-Helmut Niller, Ferenc Banati, Janos Minarovits. Epigenetic alterations in nasopharyngeal carcinoma and Epstein-Barr virus (EBV) associated gastric carcinoma: a lesson in contrasts. Journal of NasoPharyngeal Carcinoma. 2014; (9):1.

Chicago/Turabian Style

Niller Hans-Helmut; Banati Ferenc; Minarovits Janos; Hans-Helmut Niller; Ferenc Banati; Janos Minarovits. 2014. "Epigenetic alterations in nasopharyngeal carcinoma and Epstein-Barr virus (EBV) associated gastric carcinoma: a lesson in contrasts." Journal of NasoPharyngeal Carcinoma , no. 9: 1.

Journal article
Published: 01 November 2013 in Future Virology
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Hans Helmut Niller; Ferenc Banati; Katalin Nagy; Krisztina Buzas; Janos Minarovits. Update on microbe-induced epigenetic changes: bacterial effectors and viral oncoproteins as epigenetic dysregulators. Future Virology 2013, 8, 1111 -1126.

AMA Style

Hans Helmut Niller, Ferenc Banati, Katalin Nagy, Krisztina Buzas, Janos Minarovits. Update on microbe-induced epigenetic changes: bacterial effectors and viral oncoproteins as epigenetic dysregulators. Future Virology. 2013; 8 (11):1111-1126.

Chicago/Turabian Style

Hans Helmut Niller; Ferenc Banati; Katalin Nagy; Krisztina Buzas; Janos Minarovits. 2013. "Update on microbe-induced epigenetic changes: bacterial effectors and viral oncoproteins as epigenetic dysregulators." Future Virology 8, no. 11: 1111-1126.

Review
Published: 05 September 2013 in Aids Reviews
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Eva Ay; Ferenc Banati; Maria Mezei; Agnes Bakos; Hans Helmut Niller; Krisztina Buzás; Janos Minarovits. Epigenetics of HIV infection: promising research areas and implications for therapy. Aids Reviews 2013, 15, 1 .

AMA Style

Eva Ay, Ferenc Banati, Maria Mezei, Agnes Bakos, Hans Helmut Niller, Krisztina Buzás, Janos Minarovits. Epigenetics of HIV infection: promising research areas and implications for therapy. Aids Reviews. 2013; 15 (3):1.

Chicago/Turabian Style

Eva Ay; Ferenc Banati; Maria Mezei; Agnes Bakos; Hans Helmut Niller; Krisztina Buzás; Janos Minarovits. 2013. "Epigenetics of HIV infection: promising research areas and implications for therapy." Aids Reviews 15, no. 3: 1.

Case reports
Published: 03 July 2013 in BMC Infectious Diseases
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Arthropod-borne viral encephalitis of diverse origins shows similar clinical symptoms, histopathology and magnetic resonance imaging, indicating that the patho mechanisms may be similar. There is no specific therapy to date. However, vaccination remains the best prophylaxis against a selected few. Regardless of these shortcomings, there are an increasing number of case reports that successfully treat arboviral encephalitis with high doses of intravenous immunoglobulins.

ACS Style

Daniel Růžek; Gerhard Dobler; Hans Helmut Niller. May early intervention with high dose intravenous immunoglobulin pose a potentially successful treatment for severe cases of tick-borne encephalitis? BMC Infectious Diseases 2013, 13, 1 -306.

AMA Style

Daniel Růžek, Gerhard Dobler, Hans Helmut Niller. May early intervention with high dose intravenous immunoglobulin pose a potentially successful treatment for severe cases of tick-borne encephalitis? BMC Infectious Diseases. 2013; 13 (1):1-306.

Chicago/Turabian Style

Daniel Růžek; Gerhard Dobler; Hans Helmut Niller. 2013. "May early intervention with high dose intravenous immunoglobulin pose a potentially successful treatment for severe cases of tick-borne encephalitis?" BMC Infectious Diseases 13, no. 1: 1-306.

Journal article
Published: 01 January 2013 in Journal of Cancer Therapy
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MicroRNAs (miRNAs) are posttranscriptional regulators fine-tuning the level of most messenger RNAs (mRNAs) and proteins in mammalian cells. Their expression is dysregulated in neoplastic cells and upregulated or downregulated miRNAs play an important role in tumorigenesis. Changes in the miRNA transcriptome appear to be suitable markers for the differential diagnosis of various B-cell lymphoma types and there are therapeutic attempts to normalize the expression level of key cellular miRNAs involved in lymphomagenesis. In this review we wish to outline the most recent developments in the application of sophisticated, chemically modified antisense oligonucleotides and their nanoparticle complexes to suppress oncogenic miRNAs. These advances form the basis of a new therapeutic approach that may complement current protocols for B-cell lymphoma therapy. Anti-cytokine therapy aiming at the removal of cytokines that activate key oncomirs, and switching on silenced tumor suppressor miRNAs by epigenetic drugs might also be considered, on the long run, in the treatment of well defined B-cell lymphoma types.

ACS Style

Kalman Szenthe; Katalin Nagy; Krisztina Buzas; Hans Helmut Niller; Janos Minarovits. MicroRNAs as Targets and Tools in B-Cell Lymphoma Therapy. Journal of Cancer Therapy 2013, 04, 466 -474.

AMA Style

Kalman Szenthe, Katalin Nagy, Krisztina Buzas, Hans Helmut Niller, Janos Minarovits. MicroRNAs as Targets and Tools in B-Cell Lymphoma Therapy. Journal of Cancer Therapy. 2013; 04 (03):466-474.

Chicago/Turabian Style

Kalman Szenthe; Katalin Nagy; Krisztina Buzas; Hans Helmut Niller; Janos Minarovits. 2013. "MicroRNAs as Targets and Tools in B-Cell Lymphoma Therapy." Journal of Cancer Therapy 04, no. 03: 466-474.